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. 2021 Jul 1:1762:147450.
doi: 10.1016/j.brainres.2021.147450. Epub 2021 Mar 25.

The association of traumatic brain injury, gut microbiota and the corresponding metabolites in mice

Affiliations

The association of traumatic brain injury, gut microbiota and the corresponding metabolites in mice

Shenhao Wang et al. Brain Res. .

Abstract

Background: Traumatic Brain Injury (TBI) present a significant burden to global health. Close association and mutual regulation exist between the brain and gut microbiota. In addition, metabolites may play an important role as intermediary mediators of the brain and gut microbiota. Consequently, the study sought to investigate the alterations in gut microbiota and metabolites after TBI and conducted a comprehensive analysis of the correlation between gut microbiota and metabolites after TBI in mice.

Methods: Changes in intestinal microbiota and metabolites in mice after moderate or severe traumatic brain injury were detected through 16S rDNA sequencing and the non-target LC-MS technology. Additionally, Pearson correlation analysis was used to explore the association between the microbiota and metabolites.

Results: TBI was able to change the composition of intestinal microbiota, resulting to a decrease in microbial diversity in the intestinal tract (sham vs sTBI: 8.35 ± 0.12 vs 7.71 ± 0.5, p < 0.01; sTBI vs mTBI: 7.71 ± 0.5 vs 8.25 ± 0.34, p < 0.05). The results also showed that TBI could change the types and abundance of metabolites (723 in mTBI and sham groups; 1221 in sTBI and sham groups; 324 in mTBI and sTBI groups). Moreover, some of the altered gut metabolites were significantly correlated with part of the altered gut microbes after TBI.

Conclusions: TBI significantly changed intestinal microbiota as well as metabolites. Some of the altered microbiota and metabolites had a significant association. The results from this study provide information that paves way for future studies utilizing the brain gut axis theory in the diagnosis and treatment of TBI.

Keywords: Brain injury; Controlled cortical impact; Intestinal flora; Metabolites; Non-target LC-MS.

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